REDUCED CORONARY VASODILATOR FUNCTION IN INFARCTED AND NORMAL MYOCARDIUM AFTER MYOCARDIAL-INFARCTION
REDUCED CORONARY VASODILATOR FUNCTION IN INFARCTED AND NORMAL MYOCARDIUM AFTER MYOCARDIAL-INFARCTION
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DOI：
10.1056/nejm199407283310402
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发表时间：
1994-07-28
影响因子：
158.5
通讯作者：
MASERI, A
中科院分区：
文献类型：
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作者：
UREN, NG;CRAKE, T;MASERI, A
背景。冠状动脉疾病时，冠状动脉血管床扩张从而增加心肌血流量的能力可能受损，即使是由血管造影正常的冠状动脉供应的心肌区域也可能受损。这种血管舒缩功能障碍如果在急性心肌梗死后出现或加重，可能会影响非梗死直接损伤区缺血坏死的程度。我们研究了13例接受溶栓治疗的单支冠状动脉疾病患者（平均[+/-SD]年龄，62+/-11岁）。使用正电子发射断层扫描（PET）与氧-15标记水，我们测量了在基础条件下和静脉注射双吡啶达摩（0.5 mg / kg体重，4分钟）后的局部心肌血流量，所有13例患者梗死后8+/-3天（1周研究），13例患者中9例梗死后6+/-2个月（6个月研究）。在这两种情况下，我们都测量了梗死区和远离梗死区并由正常动脉供应的心肌区域的血流量。在为期一周的PET研究中，冠状动脉血管扩张剂反应（给药后心肌血流量与基础血流量之比）在梗死相关动脉为1.12+/-0.50，在远端区域为1.53+/-0.36 （P = 0.015）。在为期6个月的研究中，梗死区冠脉扩张剂反应为1.42+/-0.37，远端区冠脉扩张剂反应为2.19+/-0.69（与梗死区比较，P = 0.004；与远端区比较，1周研究中P = 0.011）。10例有单支冠状动脉疾病但无心肌梗死证据的对照患者，远端心肌值仍低于相似区域（3.17+/-0.72;P = 0.009）。急性心肌梗死后，不仅梗死心肌的阻力血管出现严重的血管舒张异常，正常冠状血管灌注的心肌也出现严重的血管舒张异常。这种功能障碍可能影响冠状动脉闭塞后心肌缺血坏死的程度。
Background. The ability of the coronary vascular bed to dilate and thus increase blood flow to the myocardium may be impaired in coronary artery disease, even regions of myocardium supplied by an angiographically normal coronary artery. If this kind of vasomotor dysfunction was present or accentuated after acute myocardial infarction, it might influence the extent of ischemia and necrosis in areas not directly injured by the infarction.Methods. We studied 13 patients (mean [+/-SD] age, 62+/-11 years) with single-vessel coronary artery disease after they had received thrombolytic therapy for myocardial infarction. Using positron-emission tomography (PET) with oxygen-15-labeled water, we measured regional myocardial blood flow under basal conditions and after the intravenous administration of dipyridamole (0.5 mg per kg of body weight over a period of four minutes) 8+/-3 days after infarction in all 13 patients (1-week study) and 6+/-2 months after infarction in 9 of the 13 (6-month study). On both occasions we measured blood flow both in the infarcted region and in a region of myocardium that was remote from the infarcted region and supplied by a normal artery.Results. At the one-week PET study, the coronary vasodilator response (the ratio of the myocardial blood flow after the administration of dipyridamole to basal blood flow) was 1.12+/-0.50 in the infarct-related artery and 1.53+/-0.36 in the remote region (P = 0.015). At the six-month study, the coronary vasodilator response was 1.42+/-0.37 in the infarcted region and 2.19+/-0.69 in the remote region (P = 0.004 for the comparison with the infarcted region; P = 0.011 for the comparison with the remote region at the one-week study). The value in remote myocardium remained lower than that in similar regions in 10 control patients, who had single-vessel coronary artery disease but no evidence of myocardial infarction (3.17+/-0.72; P = 0.009).Conclusions. After acute myocardial infarction, there is a severe vasodilator abnormality involving not only resistance vessels in infarcted myocardium, but also those in myocardium perfused by normal coronary vessels. This dysfunction may affect the extent of myocardial ischemia and necrosis after coronary occlusion.